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Systems Modelling of EMT Cell Signalling Pathways in Heart Valve Development

Systems Modelling of EMT Cell Signalling Pathways in Heart Valve Development. Tariq Abdulla 1 , Ryan Imms 1 , Jean-Marc Schleich 2 and Ron Summers 1 VPH 2010 01/10/2010. 1 Dept. Electronic and Electrical Engineering, SEIC, Loughborough University, LEICS, UK, LE11 3TU

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Systems Modelling of EMT Cell Signalling Pathways in Heart Valve Development

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  1. Systems Modelling of EMT Cell Signalling Pathways in Heart Valve Development Tariq Abdulla1, Ryan Imms1, Jean-Marc Schleich2 and Ron Summers1 VPH 2010 01/10/2010 1Dept. Electronic and Electrical Engineering, SEIC, Loughborough University, LEICS, UK, LE11 3TU E-mail: T.Abdulla@lboro.ac.uk Web: http://www-staff.lboro.ac.uk/~elta2 2LTSI, University of Rennes 1, Rennes, F-35000, France

  2. “Epithelial to Mesenchymal Transition”

  3. Outline • Heart Development – what happens? • Heart Looping • Neural Crest Cell Migration • Endocardial Cushion Growth • Congenital Heart Defects • Systems Modelling - how do we do it? • Conceptual Model • Network Modelling • Tissue Modelling • Integration • Conclusion and Future Work

  4. Heart Development: what happens? Rear View

  5. Membranous Septum Muscular Septum

  6. Neural Crest Cell Migration

  7. Endocardial Cushion Growth

  8. Heart Development: what happens?

  9. Systems Modelling – how do we do it? Different types of computational model are suitable for different levels of biological scale E.g. Biochemical reactions can be represented as networks or ODEs. Cellular behaviour can be modelled with agent based models. Use models at one level of scale, to pass information to models at another level of scale

  10. Conceptual Modeling

  11. Network Modelling KEGG

  12. Notch Signalling

  13. Notch Signalling

  14. Tissue Modelling • Tissues are often modelled as though they are continuous • But many of the interesting things that happen in tissues are to do with individual cell behaviour, and social behaviour (structure) • When there is an abnormality at tissue level we may need to know whether this is hypotrophic (fewer cells) or hypoplastic (smaller cells)

  15. Tissue Modelling • A lot of the movement of cells around each other, and how they interact, can be explained by their relative adhesiveness to other cells • This is the Differential Adhesion Hypothesis

  16. Compucell3D

  17. Compucell3D

  18. Integration • We take a proactive approach in model annotation, and are even developing methods for multiscale annotation • This includes combining terms from multiple reference ontologies in post-composition • Use of common formats such as SBML

  19. Ontologies Molecules Cells ? Tissues PMR2 Organs

  20. Conclusion and Future Work Modelling systems of such complexity is difficult, but it’s essential if we are to understand them Comparison with in vivo or in vitro data is essential for model validation and improvement This project has the potential to be applied to tissue engineering

  21. Questions or suggestions?

  22. Thanks to (in no order): Ron Summers Ryan Imms Jean-Marc Schleich Fanny Bajolle Lucile Houyel

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